title: Inhibition of pulmonary eosinophilia in P-selectin- and ICAM-1-deficient mice.
abstract: Adhesion molecule expression by pulmonary endothelial cells is considered to play an important role in the recruitment of circulating leukocytes to sites of inflammation in the lung. We have used P-selectin- and intercellular adhesion molecule type 1 (ICAM-1)-deficient mice to determine whether these adhesion molecules are important to pulmonary eosinophil recruitment after allergen challenge. There was a significant inhibition of lung tissue eosinophil recruitment in ICAM-1-deficient mice (approximately 84% inhibition compared to wild-type mice) and P-selectin-deficient mice (approximately 67% inhibition compared to wild-type mice) 3 h after allergen challenge. The number of bronchoalveolar lavage (BAL) eosinophils in P-selectin-deficient and ICAM-1-deficient mice was also significantly reduced compared with wild-type mice. Levels of BAL eosinophil peroxidase (EPO) were significantly lower in ICAM-1-deficient mice (0.21 +/- 0.03 EPO units) compared with wild-type mice (3.34 +/- 0.65 EPO units). There was no significant difference in the degree of inhibition of eosinophil recruitment in ICAM-1-deficient mice at the three time points (3, 12, and 24 h) of study after allergen challenge. However, in P-selectin-deficient mice there was a decline in the degree of inhibition of eosinophil recruitment from 3 h (67% inhibition) and 12 h (72% inhibition) postchallenge, to 24 h postchallenge (38% inhibition), suggesting that other adhesion molecules may be playing a more prominent role than P-selectin at later time points. These studies suggest an important role for ICAM-1 and P-selectin in eosinophil recruitment to the lung after allergen challenge.
authors.affiliation: Department of Medicine, University of California at San Diego, 92093-0635, USA. dbroide@ucsd.edu
authors.forename: D H
authors.initials: DH
authors.lastname: Broide
authors.forename: S
authors.initials: S
authors.lastname: Sullivan
authors.forename: T
authors.initials: T
authors.lastname: Gifford
authors.forename: P
authors.initials: P
authors.lastname: Sriramarao
mesh_terms: D000818:Animals; D000941:Antigens / Q000276:immunology; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology*; D002634:Chemotaxis, Leukocyte; D004195:Disease Models, Animal; D047209:Eosinophil Peroxidase; D004804:Eosinophils / Q000201:enzymology; D005260:Female; D006969:Hypersensitivity, Immediate; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics / Q000276:immunology*; D008168:Lung / Q000276:immunology; D051379:Mice; D008817:Mice, Mutant Strains; D010047:Ovalbumin / Q000276:immunology; D019007:P-Selectin / Q000235:genetics / Q000276:immunology*; D010544:Peroxidases / Q000032:analysis; D011657:Pulmonary Eosinophilia / Q000139:chemically induced / Q000276:immunology*; D012867:Skin / Q000276:immunology
chemical_list: D000941:Antigens; D019007:P-Selectin; D018799:Intercellular Adhesion Molecule-1; D010047:Ovalbumin; D047209:Eosinophil Peroxidase; D010544:Peroxidases